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Monday, December 12, 2016

Study group discussion: Skeletal resistance to PTH in CRF

Hi guys! So the question that was asked in the study group is- Why is there skeletal resistance to PTH in Chronic Kidney Disease?

Answer-

Skeletal Resistance to PTH has a multifaceted pathogenesis; the most imp factor being uraemia which screws with the PTH receptor's intracellular G-protein signaling mechanism in the Osteoblasts.

Dialysis in these patients increase the levels of Osteoprotegerin, which is a decoy molecule antagonizing the action of RANKL in promoting osteoclastogenesis; further intereference with the action of PTH.

Hyperphosphatemia and Hypocalcemia in CKD patients cause excessive release of PTH which leads to downregulation of its receptors on osteoblasts.

Decreased levels of calcitriol screws in a special way, it makes the parathyroid gland think that the normal calcium level range is above the actual normal value, making the gland work overtime. For this we use calcimimetics like cinacalcet to decrease the set point back to the real normal value. And also without Calcitriol to assist, PTH's job becomes a lot more difficult.

Earlier the most common CKD-related osteodystrophy was osteitis fibrosa cystica which was due to very high PTH levels causing pathologically increased bone turnover.

But now since we have developed drugs to tackle increased PTH levels, Adynamic Bone Disease has become the most common osteodystrophy because in the body of a CKD patient, it is already very difficult for PTH to carry out its function and if we are pharmacologically decreasing its values, we are ensuring that it works negligibly.

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